1. The document discusses various troubleshooting issues that can occur with cardiac implantable electronic devices (CIEDs) such as pacemakers, including implant-related issues, lead-related issues, and pacemaker malfunctions.
2. Early complications after pacemaker implantation include pneumothorax, hematoma, and lead perforation or dislodgement. Pneumothorax risk factors include procedures using the subclavian vein approach and patient characteristics like female gender, older age, COPD history.
3. Lead-related problems include dislodgement, fracture, and insulation failures. Diagnosis involves chest x-rays and device interrogation. Treatment requires lead repositioning or replacement.
The number of patients with implantable devices continues to grow. There are important aspects and difficulties in the perioperative management of these patients.
The number of patients with implantable devices continues to grow. There are important aspects and difficulties in the perioperative management of these patients.
Bradyarrhythmias, AV conduction block, Congenital complete heart block (CHB)- normal or abnormal heart structure L-Transposition (corrected transposition) Bundle of His long; AV node anterior Prone to CHB Trauma- surgical or other Slow sinus or junctional rhythm, Suppression of ectopy, Permanent pacer malfunction Drugs, electrolyte imbalances, Sick Sinus Syndrome
Case scenario of a patient with idiopathic ventricular Tachycardia (VT), followed by a topic review including diagnosis and management guidelines. It is defined as Monomorphic VT in patients without any structural heart disease or coronary disease”. Classified on the basis of site of origin broadly into three different categories i.e Outflow Tract VT, Annular VT, Fascicular VT
Myval THV Transcatheter Heart Valve by Meril Life YashChopra43
Myval THV is the new generation transcatheter heart valve. Understand more about it along with its usage in TAVR/ TAVI procedure at Meril Life. Download the brochure to know more.
Coronary CTO is characterized by heavy atherosclerotic plaque burden within the artery, resulting in complete (or nearly complete) occlusion of the vessel. Although the duration of the occlusion is difficult to determine on clinical grounds, a total occlusion must be present for at least 3 months to be considered a true CTO. Patients with CTO typically have collateralization of the distal vessel on coronary angiography, but these collaterals may not provide sufficient blood flow to the myocardial bed, resulting in ischemia and anginal symptoms. CTO is clinically distinct from acute coronary occlusion, which occurs in the setting of ST-segment–elevation myocardial infarction, or subacute coronary occlusion, discovered with delayed presentation after ST-segment–elevation myocardial infarction. Clinical features and treatment considerations of these entities differ considerably from CTO.
Among patients who have a clinical indication for coronary angiography, the incidence of CTO has been reported to be as high as 15% to 30%. Patients with CTO are referred for angiography because of anginal symptoms or significant ischemia on noninvasive ischemia testing. Patients who are symptomatic will have stable exertional angina resulting from a limitation of collateral vessel flow to meet myocardial oxygen demand with stress. Of patients referred for PCI in clinical trials of CTO PCI, only 10% to 15% of patients are asymptomatic. It is likewise uncommon for patients with CTO to present with an acute coronary syndrome caused by the CTO itself.
Bradyarrhythmias, AV conduction block, Congenital complete heart block (CHB)- normal or abnormal heart structure L-Transposition (corrected transposition) Bundle of His long; AV node anterior Prone to CHB Trauma- surgical or other Slow sinus or junctional rhythm, Suppression of ectopy, Permanent pacer malfunction Drugs, electrolyte imbalances, Sick Sinus Syndrome
Case scenario of a patient with idiopathic ventricular Tachycardia (VT), followed by a topic review including diagnosis and management guidelines. It is defined as Monomorphic VT in patients without any structural heart disease or coronary disease”. Classified on the basis of site of origin broadly into three different categories i.e Outflow Tract VT, Annular VT, Fascicular VT
Myval THV Transcatheter Heart Valve by Meril Life YashChopra43
Myval THV is the new generation transcatheter heart valve. Understand more about it along with its usage in TAVR/ TAVI procedure at Meril Life. Download the brochure to know more.
Coronary CTO is characterized by heavy atherosclerotic plaque burden within the artery, resulting in complete (or nearly complete) occlusion of the vessel. Although the duration of the occlusion is difficult to determine on clinical grounds, a total occlusion must be present for at least 3 months to be considered a true CTO. Patients with CTO typically have collateralization of the distal vessel on coronary angiography, but these collaterals may not provide sufficient blood flow to the myocardial bed, resulting in ischemia and anginal symptoms. CTO is clinically distinct from acute coronary occlusion, which occurs in the setting of ST-segment–elevation myocardial infarction, or subacute coronary occlusion, discovered with delayed presentation after ST-segment–elevation myocardial infarction. Clinical features and treatment considerations of these entities differ considerably from CTO.
Among patients who have a clinical indication for coronary angiography, the incidence of CTO has been reported to be as high as 15% to 30%. Patients with CTO are referred for angiography because of anginal symptoms or significant ischemia on noninvasive ischemia testing. Patients who are symptomatic will have stable exertional angina resulting from a limitation of collateral vessel flow to meet myocardial oxygen demand with stress. Of patients referred for PCI in clinical trials of CTO PCI, only 10% to 15% of patients are asymptomatic. It is likewise uncommon for patients with CTO to present with an acute coronary syndrome caused by the CTO itself.
Dr Priya Nair is a senior intensive care specialist at Sydney's St Vincent's Hospital and an expert in managing patients with cardiac assist devices. In this talk she takes us through the key issues encountered when on managing patients with left ventricular assist devices. As LVADs are becoming more widespread, this inside know-how is invaluable to all of us. They physiology and technology involved with these devices is pretty amazing.
This is the second of two talks at the recent Sydney Intensive Network Meeting. The first talk was by Cardiologist Chris Hayward here.
Its a medical presentation describing how to approach to various cardiac arrhythmias in systematic way. Illustrated with more ECG photographs from standard sources.
When is an arrhythmia important? Can you tell, or should you always refer to a cardiologist? What are the best management strategies for common arrhythmias and are there any potential problems to be aware of? What about the “do not miss” diagnoses?
Arrhythmias are common in critically unwell patients, and may represent primary cardiac pathology, or the cardiac response to underlying pathology. Estimates for the incidence of arrhythmias in patients in the intensive care unit (ICU) vary widely. Atrial fibrillation is the most common arrhythmia in the ICU, and management varies according to patient instability, underlying comorbidities and conditions, with important features that may favour a rate-control strategy over cardioversion, or a pharmacologic cardioversion over an electrical cardioversion. Atrial tachycardias are less common, but may have important consequences, and be difficult to manage in the intensive care patient. Ventricular arrhythmias are often immediately life threatening, and may require more than an advanced life support (ALS) algorithm to effectively treat and suppress.
The mainstay of therapy for our patients in ICU is pharmacotherapy, usually with amiodarone or diltiazem, however specific circumstances may dictate the use of other antiarrhythmic drugs. Ablation therapies may offer effective treatment for ICU patients, however have risks specific to ICU patients, associated with transport, procedural risk, delay of ongoing therapies, requirement for personnel, and isolated location.
This session will outline a practical approach to diagnosis and management of common and important arrhythmias in the ICU, and will include case and ECG discussions.
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3. Early complications of pacemaker
implantation
– Pneumothorax/Hemothorax/vascular
hemorrhage/AIR Emboli
– SVT, VT/ Cardiac arrest
– Lead dislodgement/Lead perforation
4. Pneumothorax
• Absence of lung markings over the lung
field ipsilateral to the pacemaker pocket
assessed from the fluoroscopy or pre-
discharge x-ray.
• Non-puncture related, might occur at
contralateral side
6. Pneumothorax
• 0.66% (190/28,860 patients) in Danish Pacemaker
Register
– more often in women [OR 1.9],
– age >80 years [OR 1.4],
– prior history of chronic obstructive pulmonary disease
[OR 3.9]
– implantation of a dual-chamber PM [OR 1.5]
– venous access with subclavian vein puncture [OR 7.8]
– venous access with both subclavian vein puncture and
cephalic vein cut-down [OR 5.7]
– implantation in a non-university center [OR 2.1].
9. How to avoid pneumothorax
• The cephalic vein cut-down technique
should be applied whenever possible to
avoid this complication.
10. Pneumothorax nursing care
• Administer oxygen as prescribed.
• Position the client in high fowler’s position.
• Prepare for chest tube placement until the lung
has expanded fully.
• Monitor chest tube drainage system.
13. Air Emboli
• More occurs in
– Un-cooperated patients
– Under respiratory distress
– Old age
– Snoring patients
• Management
– IV resuscitation
– Raise patients’ legs
– Increase FiO2
19. Anticoagulation therapy
• Warfarin was temporarily discontinued before device
implantation when possible to achieve an INR value
of < 1.7
• Administration of LMWH was stopped 24 h before the
procedure
• Antiplatelet therapy with ASA or clopidogrel was
allowed to continue
• Treatment with warfarin was resumed after 24 h and
with LMWH after 12–24 h
21. Lead related complications
1. Lead dislodgement
Atrial > Ventricular
2. Lead fracture
3. Loss of integrity of insulation
22. Lead failure
• Development of high pacing thresholds
or sensing problems resulting in the
need to program the device to a
different pacing mode or the need for
reoperation.
27. Lead Dislodgement
Diagnostic features
– changes in the morphology of
capture beats
– changes in dipole of the
pacing stimulus
– changes in the lead position
identified on a chest
radiograph
28. Lead Dislodgment
Treatment
– surgical intervention to reposition the lead
• an adequate heel on the intracardiac portion of the lead
• look for a 2 to 3mV current of injury pattern
• electrical and mechanical stability of the lead may be
assessed
– Twiddler’s syndrome
• the portion of the lead within the pocket should be
carefully inspected.
• If damage to the conductor coil or insulation is noted, the
lead should not be reused.
29. Order a Chest X-ray
The chest x-ray revealed a dislodged lead
40. Undersensing . . .Overpacing
• Pacemaker does not “see” the intrinsic
beat, and therefore does not respond
appropriately
Intrinsic beat
not sensed
Scheduled pace
delivered
VVI / 60
41. Inhibition of the pacemaker by events
pacemaker should ignore, e.g. EMI,
T-waves and myopotentials
Oversensing
42. Oversensing
Possible Causes Corrective Measures
•Fractured/dislodged lead •Replace/reposition lead
•Environmental interference •Eliminate interference
•T-wave oversensing •Sensing test/decrease sensitivity
•Faulty cable connections •Check connections
43. Oversensing …Underpacing
• An electrical signal other than the
intended P or R wave is detected
Marker channel
shows intrinsic
activity...
...though no
activity is present
VVI / 60